目录号 | 产品详情 | 靶点 | |
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T37050 | |||
MPS1/TTK inhibitor is an inhibitor of monopolar spindle 1 (MPS1/TTK; IC50 = 5.8 nM), a kinase involved in mitotic spindle checkpoint signaling that is overexpressed in certain cancerous tumors. It inhibits MPS1 phosphorylation of kinetochore scaffold 1 (KNL1) and increases the rate of mitosis and the number of cells entering anaphase within 15 minutes, indicating MPS1 checkpoint inhibition, when used at a concentration of 100 nM. MPS1/TTK inhibitor (50 and 100 nM) increases the number of missegregated chromosomes, with an increased number of errors at 100 nM compared with 50 nM. It also inhibits colony formation of DLD1, HCT116, and U2OS cells (IC50s = 24.6, 20.1, and 20.6 nM, respectively). | |||
T36645 | |||
CAY10763 is a dual inhibitor of indolamine 2,3-dioxygenase 1 (IDO1; IC50= 46 nM) and STAT3 activation.1It binds to STAT3 (Kd= 530 nM) and selectively reduces the levels of STAT3 phosphorylated at the tyrosine in position 705 (STAT3Y705) over phosphorylated STAT3S727, STAT1, and STAT5 in SKOV3 cells when used at a concentration of 500 nM. It also inhibits STAT3 nuclear translocation in SKOV3 cells. CAY10763 is cytotoxic to HCT116, SKOV3, A549, and HepG2 cancer cells (IC50s = 37, 28, 33, and 12 nM, respectively). It reduces tumor growth in B16/F10 mouse melanoma and HepG2 mouse xenograft models when administered at doses of 100 and 10 mg/kg, respectively. 1.Huang, R., Jing, X., Huang, X., et al.Bifunctional naphthoquinone aromatic amide-oxime derivatives exert combined immunotherapeutic and antitumor effects through simultaneous targeting of indoleamine-2,3-dioxygenase and signal transducer and activator of transcription 3J. Med. Chem.63(4)1544-1563(2020) | |||
T36321 | |||
C6 urea ceramide is an inhibitor of neutral ceramidase.1 It increases total ceramide levels in wild-type mouse embryonic fibroblasts (MEFs) and in HT-29 colon cancer cells but not in MEFs lacking neutral ceramidase. It inhibits proliferation of, and induces apoptosis and autophagy in HT-29, but not non-cancerous RIE-1, cells when used at concentrations of 5 and 10 μM. C6 urea ceramide decreases total β-catenin, increases phosphorylated β-catenin, and induces colocalization of β-catenin with the 20S proteasome in HT-29 and HCT116, but not RIE-1, cells. It reduces tumor growth and increases C16, C18, C20, and C24 ceramide levels in tumor tissue in an HT-29 mouse xenograft model when administered at doses of 1.25, 2.5, and 5 mg/kg for five days. |1. García-Barros, M., Coant, N., Kawamori, T., et al. Role of neutral ceramidase in colon cancer. FASEB J. 30(12), 4159-4171 (2016). | |||
T36630 | |||
MRTX9768 hydrochloride is a potent, orally active PRMT5 inhibitor. MRTX9768 hydrochloride is a synthetic lethal-based inhibitor binding the PRMT5-MTA complex[1]. MRTX9768 inhibits SDMA and cell proliferation in HCT116 MTAP-del cells (SDMA IC50 3 nM; prolif. IC50 11 nM) with marked selectivity over HCT116 MTAP-WT cells (SDMA IC50 544 nM; prolif. IC50 861 nM)[1].MRTX9768 selectively targets MTAP/CDKN2A-deleted tumors[2][1]. In xenograft studies, oral administration of MRTX9768 demonstrates dose-dependent inhibition of SDMA in MTAP-del tumors, with less SDMA modulation observed in bone marrow[1]. [1]. Christopher R. Smith, et al. Abstract LB003: Fragment based discovery of MRTX9768, a synthetic lethal-based inhibitor designed to bind the PRMT5-MTA complex and selectively target MTAP/CDKN2A-deleted tumors. AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA.[2]. Yingqing Chen, et al. Targeting protein arginine methyltransferase 5 in cancers: Roles, inhibitors and mechanisms. Biomed Pharmacother. 2021 Oct 4;144:112252. | |||
T73515 | Apoptosis HDAC | ||
MC2590 是一种具有有效性和选择性的组蛋白脱乙酰酶 (HDAC) 抑制剂 ,抑制 HDAC1-3、-6、-8 和 -10 的活性,诱导细胞周期停滞,促进细胞凋亡。 | |||
T36846 | |||
Chromomycin A2 is an aureolic acid that has been found in several marine actinomycetes and has antibacterial and anticancer activities. Chromomycin A2 inhibits the growth of B. subtilis in an agar diffusion assay. It also inhibits the growth of human SGC7901 gastric cancer, HepG2 hepatocellular carcinoma, A549 lung epithelial adenocarcinoma, HCT116 colon cancer, and COC1 ovarian cancer cells, as well as human umbilical vein endothelial cells (HUVECs; IC50s = 4, 0.5, 3, 5, 5, and 8 nM, respectively). Chromomycin A2 (30 nM) halts the cell cycle in the G0/G1 phase and increases the protein levels of LC3A and LC3B in MALME-3M melanoma cells, indicating that it induces autophagy. It also increases the levels and promoter activity of the autophagic proteins ATG7 and ATG10 and reduces cell viability to 50% in human SCC-11 squamous cell carcinoma cells when used at a concentration of 30 nM. | |||
T65994 | |||
Wnt signaling is required for direct multiple biological processes and also plays key roles in the pathogenesis of various diseases. Cyclic AMP response element-binding protein (CREB) is a transcription factor that is a member of the leucine zipper family of DNA binding proteins. This protein binds as a homodimer to the cAMP-responsive element, an octameric palindrome. The protein is phosphorylated by several protein kinases, and induces transcription of genes in response to hormonal stimulation of the cAMP pathway. Via generating a transcriptionally active complex with β-catenin, CREB acts as a mediator of Wnt signaling.ICG-001 is an inhibitor of β-catenin/CREB mediated transcription. The direct cellular target of ICG-001 is CREB. the inhibitory IC50of ICG-001 against β-catenin/CREB mediated transcription was 3 μM. ICG-001 treatment at the concentration of 25 μM for 24h significantly increased caspase activity in both colon cancer cell lines SW480 and HCT116 cell lines but not in normal colonic epithelial cells CCD-841Co. In a cell growth inhibition assay, the IC50s of ICG-001 against SW480 and HCT116 cells were 4.43 μM and 5.95 μM, respectively.In a SW620 nude mouse xenograft model, an water-soluble analog of ICG-001 given at the dose of 150 mg/kg i.v. once in every 2 days dramatically suppressed tumor growth. In a bleomycin-induced pulmonary fibrosis mice model, ICG-001 given at the dose of 5 mg/kg per day reversed pulmonary fibrosis. In a rat myocardial infarction model, ICG-001 was administrated subcutaneously at the dose of 50 mg/kg/day for 10 days which significantly improved cardiac contractile function after myocardial infarction in the rats. | |||
T35687 | |||
Collismycin A is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities, including antibacterial, antiproliferative, and neuroprotective properties. It is active against a variety of bacteria (MICs = 6.25 and 100 μg/ml) and fungi (MICs = 12.5-100 μg/ml). It inhibits proliferation of A549 lung, HCT116 colon, and HeLa cervical cancer cells (IC50s = 0.3, 0.6, and 0.3 μM, respectively) and NIH373 fibroblasts (IC50 = 56.6 μM) but not MDA-MD-231 breast cancer cells (IC50 = >100 μM). Collismycin A forms a complex with Fe(II) and Fe(III) at a 2:1 ratio, and the addition of iron ions inhibits the antiproliferative effect of collismycin A on HeLa cells, an effect that does not occur with the addition of zinc, manganese, copper, or magnesium ions. Collismycin A (1 μM) prevents apoptosis in the brain region of zebrafish larvae by 44% in a model of neuronal cell death induced by all-trans retinoic acid . |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04023 | BCCIP Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein that has been implicated in maintenance of genomic stability, cell cycle regulation, and microtubule dynamics. The secondary genetic alternations may overcome the progression suppression imposed by BCCIP deficiency through a synthetic viability mechanism. Knockdown of YY1 inhibited the binding of BCCIP itself at BCCIP promoter region proximal to TSS, demonstrating that transcriptional regulation of the YY1 on BCCIP can be modulated by BCCIP itself in a YY1-dependent fashion. BCCIP (BRCA2 and CDKN1A interacting protein) plays a critical role in maintaining the critical functions of p53 in tumor suppression and response to therapy. Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner.
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TMPY-00578 | BCCIP Protein, Human, Recombinant | Human | Baculovirus-Insect Cells | ||
BCCIP was originally identified as a BRCA2 and CDKN1A interacting protein that has been implicated in maintenance of genomic stability, cell cycle regulation, and microtubule dynamics. The secondary genetic alternations may overcome the progression suppression imposed by BCCIP deficiency through a synthetic viability mechanism. Knockdown of YY1 inhibited the binding of BCCIP itself at BCCIP promoter region proximal to TSS, demonstrating that transcriptional regulation of the YY1 on BCCIP can be modulated by BCCIP itself in a YY1-dependent fashion. BCCIP (BRCA2 and CDKN1A interacting protein) plays a critical role in maintaining the critical functions of p53 in tumor suppression and response to therapy. Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner.
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